资源描述:
《BAG-1-CDK4蛋白在结直肠癌中的表达及意义.doc》由会员上传分享,免费在线阅读,更多相关内容在工程资料-天天文库。
1、BAG-1CDK4蛋白在结氏肠癌屮的表达及意义[摘要]目的:探讨BAG-1、CDK4蛋白在结肓肠癌屮的表达及其与结肓肠癌临床病理特征的关系。方法:应用免疫纟H•化SP法对80例结岚肠癌纟H织、40例结真肠腺瘤纟H.织及25例癌旁正常结育肠组织屮的BAG-kCDK4进行检测。结果:BAG-kCDK4在结直肠癌屮过度表达,阳性率分别为80.0%(64/80)和65.0%(52/80),并且BAG-1、CDK4与肿瘤的分化程度成反比。有淋巴结转移的结育肠癌BAG-kCDK4的阳性率分别为96.7%(29/30)
2、和83.3%(25/30),无淋巴结转移的结育肠癌阳性率分别为70.0%(35/50)和54.0%(27/50),两者比较,差异有高度统计学意义(P<0.01)o侵及浆膜层者CDK4蛋白表达阳性率明显高于未侵及浆膜层者,阳性率分别为71.4%(40/56)和35.3%(12/34),差异有高度统计学意义(P<0.01)。结论:BAG-l、CDK4的过度表达与肿瘤的分化程度、淋巴结转移密切相关;CDK4的过度表达还与浸润深度密切相关;结直肠癌的发生机制涉2^BAG-kCDK4调节环路屮多个基因的异常。[关键词
3、]结真肠癌;BAG-1蛋白;CDK4蛋白;免疫组织化学[中图分类号]R735.3+7[文献标识码]A[文章编号]1673-7210(2010)03(a)-016-03ExpressionandsignificoneeofBAG-1andCDK4inthecolorectaicancerZHANGZhaoxial,LIANGJianfang2,ZHENGHuixia2,XIAOHong2(1.DivisionofPathology,FenyangCollegeofShanxiMedicalUniversity
4、,Fenyang032200,China;2.DepartmentofPathology,theFirstClinicalMedicalCollegeofShanxiMedicalUniversity,Taiyuan030001,China)[Abstract]Objective:ToexploretheexpressionsofBAG-1“ndCDK4proteinincolorectalcanceranditsrelationshipwithclinicopathologicalfeaturesofco
5、lorectalcancer.Methods:BAG-1anclCDK4proteinweredetectedin80casesofcolorectalcancer,40casesofcolorectaladenomasand25casesofadjacentnormalcolorectaitissuesbyimmunohistochemistrySPmethod.ResuIts:TheoverexpressionofBAG-1anclCDK4incolorectalcancerwere80.0%(64/8
6、0)and65.0%(52/80)respectively,BAG-1andCDK4wereinverselyproportionaltothedegreeoftumordifferentiation.ThepositiveratesofBAG-1andCDK4were96.7%(29/30)ancl83.3%(25/30)inlymphnodemetastasisofcolorectalcancer,andwere70.0%(35/50)ancl54.0%(27/50)innolymphnodemetas
7、tasisofcolorectalcancer,theyshowedsignificantdifference(P<0.01).CDK4proteinexpressioninserosalinvasionwassignificantlyhigherthanthoselessthanserosallayer,thepositiverateswere35.3%(12/34)and71.4%(40/56)respectively,theywerestatisticallysignificant(P<0.01).C
8、onclusion:TheoverexpressionofBAG-1andCDK4showsagoodcorrelationwithtumordifferentiationand1ymphnodemetastasis.TheoverexpressionofCDK4iscloselyrelatedwiththedepthofinvasion.Abnormalityofmanygenesintheregulatory